Abstract
Typhus group rickettsiosis is caused by the vectorborne bacteria Rickettsia typhi and R. prowazekii. R. typhi, which causes murine typhus, the less severe endemic form of typhus, is transmitted by fleas; R. prowazekii, which causes the severe epidemic form of typhus, is transmitted by body lice. To examine the immunology of human infection with typhus group rickettsiae, we retrospectively reviewed clinical signs and symptoms, laboratory changes, and travel destinations of 28 patients who had typhus group rickettsiosis diagnosed by the German Reference Center for Tropical Pathogens, Hamburg, Germany, during 2010–2017. Immunofluorescence assays of follow-up serum samples indicated simultaneous seroconversion of IgM, IgA, and IgG or concurrence in the first serum sample. Cytokine levels peaked during the second week of infection, coinciding with organ dysfunction and seroconversion. For 3 patients, R. typhi was detected by species-specific nested quantitative PCR. For all 28 patients, R. typhi was the most likely causative pathogen.
Highlights
Typhus group rickettsiosis is caused by the vectorborne bacteria Rickettsia typhi and R. prowazekii
Cases and Inclusion Criteria We screened the database of the German Reference Center for Tropical Pathogens at the Bernhard Nocht Institute for Tropical Medicine in Hamburg for autochthonous and imported Typhus group rickettsiosis (TGR) cases diagnosed from January 1, 2010, through December 31, 2017
We found no cases of definitive R. prowazekii infection
Summary
We identified 28 TGR patients (Table 1); age range was 4–80 years (mean age 38.3 years), and male:female ratio was 1.5:1. Three infections were locally acquired in Germany by patients without a travel history (patients 9, 15, and 21). Patients were examined on different days of illness at different hospitals. At the time of initial examination, the most frequently reported sign or symptom was fever (79%), followed by exanthema (50%; Figure 2), headache (46%), myalgia/arthralgia (25%), cough/pneumonia (15%), and splenomegaly (11%). The earliest that antibodies against TGR antigens were detected was day 7 of illness. Antibody titers of any class varied among patients despite illness onset occurring on the same day. No serologic differentiation between R. typhi and R. prowazekii was achieved by IFA; titer differences between the 2 species for all antibody classes were
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